Mitochondrial calcium sequestration in cortical and hippocampal neurons after prolonged ischemia of the cat brain.

Adult normothermic cats were submitted to 1- h complete cerebrocirculatory arrest, followed by blood recirculation for 6-8 h. Two groups of animals could be distinguished: In one group electrocorticogram and somatically evoked primary cortical potentials steadily recovered after ischemia, and in another electrophysiologic recovery was absent. At the end of the recirculation period, calcium content was measured in tissue samples taken from cerebral cortex and hippocampus, and compared with mitochondrial calcium sequestration as assessed by electron-microscopic cytochemistry. Protein content of cortex and hippocampus was also determined for evaluation of tissue swelling. The two regions were selected because previous experiments had revealed that in animals with electrophysiologic recovery cerebral cortex remains intact although hippocampus is selectively injured, whereas in animals without electrophysiologic recovery both cerebral cortex and hippocampus are damaged. In animals with functional recovery, neither calcium content nor mitochondrial calcium sequestration were significantly increased in either cerebral cortex or hippocampal subfield CA1. Only in dentate gyrus a minor degree of mitochondrial calcium sequestration was present. Calculation of tissue swelling revealed no change in cerebral cortex, but a volume increase by 18% in hippocampus, indicating development of brain edema in this region. In animals without functional recovery tissue calcium significantly increased both in cortex and hippocampus (by 49% and 73% of control, respectively), and there was significant mitochondrial calcium accumulation in both regions. Calculated brain swelling in these animals amounted to 16% and 26% in cortex and hippocampus, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)